Most late deaths after intracardiac repair of congenital heart defects such as tetralogy of Fallot (TOF) occur suddenly in children with previously documented ventricular dysrhythmias (VDS) and elevated systolic and filling pressure in the right ventricle (RV). These deaths result, presumably, from ventricular fibrillation (VFIB) initiated by conditions which increase ventricular automaticity or favor reentry. After TOF repair, these conditions might include myocardial fibrosis from the right ventriculotomy scar, residual RV hypertrophy, systolic pressure overload from persistent RV outflow obstruction, stretch from RV dilation due to pulmonary valve insufficiency, or a combination of these factors. We propose to investigate the electrophysiologic and hemodynamic mechanisms responsible for VDS and sudden death after cardiac surgery involving ventriculotomy. Our model will be a chronically-instrumented, nonsedated adult dog preparation. Chronic VDS will be detected by weekly 24-hour tape ECGs over a 10 week period in 8 groups, each with 6 dogs who have undergone instrumentation and one or more surgical procedures, including right ventriculotomy, pulmonary artery (PA) banding, and pulmonary valvectomy. Measurements will be recorded weekly: A) Hemodynamic- pressures (RV and LV systolic and end-diastolic), right main and left anterior descending coronary artery flow; B) Biochemical- serum epinephrine and norepinephrine concentrations; C) Electrophysiologic- dispersion of ventricular muscle refractory periods, ability to induce repetitive extrasystoles, ventricular escape rate after vagal stimulation and VFIB threshhold. After 10 weeks, the hearts will be removed and examined for gross and microscopic pathology. The management of patients before, during and after repair of congenital and acquired defects involving ventriculotomy could be partially determined by the results of this study. For example, if residual systolic pressure overload were a major factor associated with VDS, stricter criteria could be developed for the maximum acceptable RV systolic pressure immediately after TOF repair. These studies will also create a model which can be used in the future for studies of pharmacologic or surgical treatment of chronic PO VDS. In order to institute rational medical or surgical treatment for Po VDS, it is essential to understand the mechanisms involved.